A lack of B vitamins, especially folic acid, vitamin B6 and vitamin B12, contributes to high plasma homocsysteine levels. Elevated homocysteine levels are associated with increased risk of CHD. A proposed mechanism of action is via DNA methylation pathways. Fiorito and colleagues studied the relationship between candidate genes and B vitamin intakes in 206 individuals with previous heart attacks and 206 matched controls identified from the EPIC cohort. They found significantly lower intakes of folic acid, B6, riboflavin and niacin in cases versus controls. They also found several candidate genes with statistically different DNA-methylation patterns which were associated with CHD risk.

The cardiovascular health story isn’t restricted to B vitamins. Omega-3 fatty acid intakes are known to be important for heart health. The apolipoprotein E (APOE) gene helps make lipoproteins, primarily very low-density lipoproteins (VLDL), to remove cholesterol to the liver for processing. There are 3 genes: e2, e3, and e4. People with the e4 genotype are at increased risk of atherosclerosis and Alzheimer’s. Chouinard-Watkins and colleagues report that the metabolism of long-chain fatty acids is influenced by genetics. They evaluated the metabolism of a single oral dose (40mg) of isotopically-labeled docosahexaenoic acid (DHA) in 40 volunteers over 28d. Mean plasma labeled DHA levels were 31% lower in people expressing the apoE ε4 allele (E4+) than those without (E4-) genotype.

These 3 new papers highlight potential interactions between nutrition and genes. As genotyping becomes more commonly available, it will be applied by health professionals to personalize national nutrient recommendations to optimize the health of their client.